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Week 4/5 FMM > Energy Metabolism II > Flashcards

Energy Metabolism II Flashcards

(51 cards)

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1
Q

Where in the cell does pyruvate oxidation take place

A

Mitochondria

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2
Q

Where in the mitochondria does electron transfer/oxidative phosphorylation take place?

A

Inner membrane

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3
Q

where in the mitochondria does the TCA cycle and fatty acid oxidation take place?

A

matrix

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4
Q

How does pyruvate get into the matrix of the mitochondria

A

through symporter that couples it with H+ movement down it’s gradient

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5
Q

pyruvate dehydrogenase

A

converts pyruvate to acetyl CoA and Co2 through oxidative decarboxylation

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6
Q

what does pyruvate dehydrogenase require to function

A

5 cofactors (mainly B vitamin derived)

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7
Q

Regulation of pyruvate dehydrogenase

A

under hormonal control and feedback regulation

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8
Q

Beriberi

A
  • deficiency in thiamin (B1)
  • decreased ability to oxidize pyruvate
  • leads to high blood pyruvate and lactate
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9
Q

arsenic poisoining

A
  • inactivates pyruvate dehydrogenase

- arsenate=robs cells of ability to make ATP

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10
Q

Acetaldehyde

A
  • metabolic product from alcohol
  • can get a lot from excessive alcohol consumption
  • inhibits pyruvate dehydrogenase
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11
Q

TCA cycle (kreb’s, citric acid)

A
  • starting substance is acetyl-coA (2 carbons)
  • 2 carbons leave as CO2
  • generates 4 pairs of electrons, one GTP that are fed into the electron transport chain to generate ATP
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12
Q

succinate dehydrogenase

A

only enzyme in TCA cycle that is embedded in mitochondrial inner membrane, the rest are in the matrix

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13
Q

substrate level phosphorylation of GTP

A

at one step in TCA cycle; when GTP is generate directly from a reaction, not indirectly

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14
Q

oxaloacetate

A

what is combined with acetyl coA at the beginning of the TCA cycle to make citrate
-can limit flux through pathway by limiting it

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15
Q

TCA intermediates can be used for what?

A

can be used for biosynthesis of amino acids, glucose, fatty acids, cholesterol, and porphyrins

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16
Q

pyruvate carboxylase

A
  • generates oxaloacetate from pyruvate

- helps replenish TCA intermediate supply

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17
Q

If NAD+ level is high, what does that do to the flux of the TCA cycle

A

Increases it because you want to create NADH for electron transport chain

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18
Q

If ADP level is high, what does that do to the flux of the TCA cycle

A

Increases it so you can get NADH and put that into electron transport chain

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19
Q

what is the ultimate acceptor of electrons in electron transport chain?

A

oxygen

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20
Q

Flavin mono nucleotide

A

carries two electrons

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21
Q

coenzyme Q

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A
  • carries up to two electrons
  • very hydrophobic so stays in mitochondrial membrane
  • collects electrons from complex 1 (NADH) but can also collect straight from FAD (just generates slightly less ATP
22
Q

cytochromes

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A

-can carry only 1 electron

23
Q

iron-sulfur proteins

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A

allow use of electrons outside the mitochondrial matrix

24
Q

complex I

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A
  • electrons from NADH reduce it and in the process it pumps 4 protons into outside matrix
  • can only accept from NADH not FAD
  • passes electrons to CoQ
25
complex III
- takes electrons from CoQ | - passes electrons to cyt c
26
complex IV
- cyt c binds to it and it oxidizes it, pulling electrons off of it and putting them on oxygen which gets reduced to water - in the process pumps 2 protons into inter membrane space
27
Inhibitors of complex IV
- azide, carbon monoxide, cyanide | - bind to complex IV at higher affinity than oxygen and poison it so it can't work at all
28
How does ATP synthase generate ATP?
- uses energy from proton moving down proton gradient to cause conformational changes that release ATP - more positive in intermembrane space, more negative in the matrix
29
ATP translocators
- move ATP from mitochondria to other parts of the cell - ADP/ATP exchange (ATP is more negative so it wants to go to the more positive inner membrane space so the two switch) - phosphate translocase (symporter) allows phosphate to flow in with proton (uses energy from proton moving down gradient) - phosphate and ADP combine to make ATP that can flow out through ADP/ATP exchange
30
What happens to electron transport chain when there is no oxygen
basically stops
31
The electron transport chain is an example of:
oxidative phosphorylation
32
Dinitrophenol (DNP)
- provides another path for protons to cross the membrane - uncouples oxidative phosphorylation in an uncontrolled way; collapses the proton gradient so you lose proton motive force and ATP synthesis halts
33
UCP/thermogenin
- uncouples oxidative phosphorylation in a controlled way - in mitochondria of brown fat (where there is a high content of mitochondria) - ATP is not generated and instead the movement of protons down their gradient generates heat
34
gluconeogenesis
- biosynthesis of glucose - occurs mainly in liver (also in kidney) - occurs during fasting (especially after depletion of glycogen), when it is the sole glucose source - requires carbon source and energy source
35
carbon source for gluconeogenesis
carbon skeletons from amino acids
36
energy source for gluconeogenesis
from fatty acid oxidation
37
metformin
inhibits gluconeogenesis | -used for type II diabetes
38
three irreversible steps of glycolysis that must be bypassed in gluconeogenesis
- hexokinase - phosphofructokinase (PFK-1) - pyruvate kinase
39
how is pyruvate kinase bypassed
through conversion of pyruvate to oxaloacetate (shuttled out of mitochondria) then to PEP
40
carbon sources for gluconeogenesis
- lactate from muscles or RBCs (converted to pyruvate by lactate dehydrogenase) - fructose and galactose - glucogenic amino acids from diet or muscle breakdown - glycerol from triglyceride breakdown
41
crucial entry point for gluconeogenesis
oxaloacetate
42
pyruvate carboxylase
converts pyruvate to oxaloacetate
43
cori cycle
converts lactate to glucose in the liver
44
glucose-alanine cycle
converts alanine to glucose in the liver (through pyruvate)
45
major carbon source for gluconeogenesis during fasting
amino acids from muscle breakdown
46
glucose-6-phosphatase
- converts glucose-6-phosphate back to glucose so it can diffuse into the blood - only liver and kidney have it
47
von Gierke disease
glucose-6-phosphatase deficiency | -patients with this need to be constantly fed some form of glucose
48
PEP carboxykinase
converts oxaloacetate to PEP | -committed step in gluconeogenesis from pyruvate/lactate
49
Fructose 2,6 bisphosphate (F26BP) regulatory function
- activates glycolysis - inhibits gluconeogenesis - concentrations high in fed state, low in fasting state
50
PFK-2
synthesizes F26BP - activated by insulin - will stimulate glycolysis
51
FBPase-2
breaks down F26BP to Fructose-6-phosphate - activated by glucagon - stimulates gluconeogenesis

Week 4/5 FMM (8 decks)

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